This document provides information on Vitamins D and K. It discusses the sources, structures, functions, recommended daily intake and deficiency symptoms of each vitamin. Vitamin D helps regulate calcium levels and bone mineralization, while Vitamin K is required for blood clotting through the gamma-carboxylation of clotting factors in the liver. Both vitamins are fat-soluble and absorbed through the intestine with dietary fats and bile salts.

1. VITAMIN D
AND
VITAMIN K
PRESENTED BY :BISHAL PATHAK
DATE : 5/1/2023
COURSE : Bsc.MLT 10TH BATCH
VENUE :BIOCHEMISTRY DEPARTMENT

2. CONTENT
 VITAMIN
 SOURCES OF VITAMIN
 FORM OF VITAMIN
 RECOMMENDED DIETARY ALLOWANCE
 STRUCTURE OF VITAMIN
BIOCHEMICAL FUNCTION OF VITAMIN
ABSORPTION , TRANSPORTATION , STORAGE
DEFICIENCY SYMPTOMS
HYPERVITAMINOSIS

3. VITAMIN D
Vitamin D is also called as cholecalciferol.
Vitamin D is a fat soluble vitamin which required fatty acid
and bile salt for it absorption in body.
. Angus and coworkers isolated vitamin D in 1931 and
named it as calciferol, which was later identified as Vitamin
D3 .
 It is also called as sun shine vitamin.

4. RDA
 Children :- 10 micro gram per day
 Adult :- 5 micro gram per day
 Pregnant and lactation :- 10 micro gram per day
 Above age of 60 year :- 600 IU
 The daily requirement of vitamin D is 400 International Units
(IU) or 10 mg of cholecalciferol.
 In countries with good sunlight (like India), the RDA for vitamin
vitamin D is 200 IU

5. Forms of vitamin D: Vitamin D in the diet occurs in
two forms ;
 Vitamin D2 (Ergocalciferol) :- Plant
 Vitamin D3 (Cholecalciferol) :- Animal
 Other sources :- Fatty fish , Fish liver oil , egg yolk
Note:- Milk is not good source of vitamin D
:- Ergocalciferol and Cholecalciferol both are the
source of vitamin D so called as provitamins.

6. Structure

7.  In the skin, ultraviolet light (290–315 nm) breaks the bond
between position 9 and 10 of the steroid ring.
 The B ring is opened, to form the provitamin, secosterol .
 The cis double bond between 5th and 6th carbon atoms, is
then isomerized to a trans double bond.
 Which give rise to vitamin D3 or cholecalciferol.

8. Absorption ,Transportation &
storage
 Vitamin D is absorbed in the small intestine for which
bile salt is essential.
 Through lymph, vitamin D enters the circulation bound
to plasma D2-globulin and is distributed throughout the
body.
 Liver and other tissues store small amounts of vitamin
D.

9. Synthesis of calcitriol (1,25-DHCC)
 Vitamins D2 and D3, are not biologically active. They are
metabolized identically in the body and converted to
active forms that is calcitriol.
 On exposure to sunlight , 7-dehydrocholesterol is
converted to cholecalciferol (D3) in the skin by the action
UV light of 290-315 nm.
 7-dehydrocholesterol is available in the epidermal layer of
skin.

10.  The cholecalciferol is first transported to liver.
 Where hydroxylation at 25th position occurs, to form 25-
hydroxy cholecalciferol (25-HCC) in presence of 25-hydeoxylase
enzyme.
 It requires cytochrome P-450 and NADPH.
 25-HCC is the major storage form of vitamin D in body.
 After that it transfer to the kidney with the help of vitamin D
binding protein (VDBP).
 In kidney, it is further hydroxylated at the 1st carbon position in
the presence of one-alpha hydroxylase enzyme.

11.  1-alpha hydroxylase is located in mitochondria of proximal
convoluted tubules.
 It requires cytochrome P- 450, NADPH and ferrodoxin.
 Thus 1, 25-dihydroxy cholecalciferol (DHCC) is formed which
is the active form of vitamin D.

13.  As 1,25-DHCC contain 3 hydroxyl group , It called as calcitriol.
 Calcitriol regulates the plasma levels of calcium and phosphate in
circulation.
 Calcitriol acts at 3 different levels (intestine, kidney and bone) to
maintain plasma calcium level in body.

15. Biochemical function
 Action of calcitriol in intestine:
 Calcitriol promotes the absorption of calcium and
phosphorus from the brush border of intestine.
 Calcium is absorbed passively , but required energy for
the absorption from intestinal cell to blood circulation.
 The transporter are Calbindin ,CaATPase ,TRPV6 in the
intestine for calcium and Na-pi 2b for phosphorus .

16.  In the intestinal cells, calcitriol binds with a calcium binding
receptor to form a calcitriol-receptor complex.
 This complex then interact with a specific DNA leading to
synthesis of a specific calcium binding protein (calbindin).
 Finally this protein increase the calcium uptake from the
intestine.

18.  Action of calcitriol on bone
 Mineralization of the bone is increased by increasing
the activity of osteoblasts.
 Calcitriol coordinates the remodeling of bone and
increases bone mineral density.
 Calcitriol stimulate osteoblast which secrete alkaline
phosphatase . Due to this enzyme , the local
concentration of phosphate increase.
 The ionic product of calcium and phosphorus
increases , leading to mineralization of bone.

19.  Action of calcitriol on the kidney
 Calcitriol is also involved in minimizing the excretion of
calcium and phosphate through the kidney, by decreasing
their excretion and enhancing reabsorption.

20. Function of calcitriol

21.  24,25-Dihydroxycholecalciferol (24,25-DHCC) is another
metabolite of vitamin D.
 The exact function of 24,25-DHCC is not known.
 When calcitriol concentration is adequate in body, 24-
hydroxylase acts on 25-DHCC leading to the synthesis of a less
important compound 24, 25-DHCC.
 The formation of 24,25-DHCC is done in kidney , by
hydroxylation at 24-th position , which is very less active.
 In this way, to maintain the homeostasis of calcium, synthesis
of 24,25-DHCC is also important.
24,25-Dihydroxycholecalciferol

22. Deficiency symptoms
 Vitamin D deficiency is relatively less common, since this
vitamin can be synthesized in the body.
 Insufficient exposure to sunlight and consumption of diet
lacking vitamin D results in its deficiency.
 Deficiency mostly seen in :
 Strict vegetarian ,
 chronic alcoholic
 kidney diseases
 Liver diseases,

23.  Defective cholesterol metabolism .
 Muslim community covers entire body with “Burka”
 Deficiency of vitamin D causes:
1. Rickets in children :-
 There is insufficient mineralization of bone. Bones become
soft and pliable (flexible) with delay in teeth formation.
 Classical features of rickets are bone deformities. Weight
bearing bones are bent.

24. Rickets

25.  Clinical feature of Rickets
 The clinical manifestations include bow legs ,pigeon chest.
 Plasma calcium and phosphorus are low.
 Mostly weight bearing bone are bent.

26. Osteomalacia
 Also called as adult rickets.
 The term is derived from Greek “osteon” = bone; and
“malakia” = softness.
 The bones are softened due to insufficient mineralization
mineralization and increased osteoporosis. Patients are
more prone to get fractures.
 Biochemical parameters are a slightly lower serum
calcium, and a low serum phosphate.

27. Renal rickets
 This is seen in patients with chronic renal failure.
 Renal rickets is mainly due to decreased synthesis of
calcitriol in kidney.
 It can be treated by administration of calcitriol.
Diagnosis of vitamin D deficiency
 Estimation of plasma level for 25-
hydroxycholecalciferol .

28. Hypervitaminosis D
 Vitamin D is most toxic in overdose
 Doses above 10,000 units per day for long periods may
cause toxicity of vitamin D.
 Toxic effects of hypervitaminosis D include
demineralization of bone.
 Increased calcium absorption from the intestine,
leading to elevated calcium in plasma (hypercalcemia)
 Prolonged hypercalcemia is associated with deposition
of calcium in many soft tissues.

29.  Hypervitaminosis D may lead to formation of stones in kidneys.
 Other symptom of hypervitaminosis D are loss of appetite,
nausea, increased thirst, loss of weigh .
 Note :- , Excessive exposure to sunlight does not result in
vitamin D toxicity.

30. Vitamin K
 Also called as coagulation vitamin ,which is required for
the synthesis of blood clotting factor essential for
coagulation.
 The letter “K” is the abbreviation of the German word
“koagulation vitamin”.
 They are heat stable and there activity is lost by
oxidizing agents , strong acid and alkalis.

31. Chemistry
 Vitamin K exists in different forms that is k1 , k2 ,k3
 K1 = phylloquinone (20c) ( present in plant)
 K2 = menaquinone(30c) (present in animal and also
produced by intestinal bacteria )
 K3 = menadione ( synthetic form of vit. K , also water
soluble and administrated as drugs to child in inactive
form to immature infant whose liver not developed well
)

32.  They are naphthoquinone derivatives, with a long
isoprenoid side chain present only in K1 and K2 .
Structure of vitamin K

33. Absorption , Transport and
storage
 Absorption takes place along with fat and bile salts.
 Vitamin K is transported along with lipoprotein.
 Stored mainly in liver and, to a lesser extent, in other
tissues .

34. Biochemical function
 Blood Coagulation
 The functions of vitamin K are concerned with blood
clotting process.
 Posttranslational modification of gamma-carboxylation
of factor II,VII,IX,X)

35.  These factor synthesize in inactive form by zymogen cell of
liver.
 Vitamin K help to convert glutamate of precursors clotting
factor to the gamma-carboxy glutamic acid with additional
negative charge (coo-) .
 Now this negative charge bind with the positive charge of
calcium ion (ca++) and help in the formation of calcium
prothrombin complex.
 Which attach to the phospholipid of platelets membrane
and help in conversion of prothrombin to thrombin.
 So that the fibrin thread is formed and bleeding stops.

37.  Vitamin K dependent gamma carboxylation is also
necessary for the functional activity of osteocalcin and
synthesis of osteocalcin.

38. Vitamin K cycle for
carboxylation reaction

39. RDA
 Adult :- 70-100 micro gram /day
 Vitamin k is adequately synthesized by intestinal
flora in gut .
 Dietary sources
 Plant source :- cabbage , tomatoes ,other green
vegetables
 Animal source :- egg yolk , meat, liver , dairy
product

40. Deficiency symptoms
 The blood clotting time increase.
Hypervitaminosis
 Administration of large doses of vitamin K
produces hemolytic anemia particularly in
infants.